Generation of wave break is a characteristic feature of cardiac fibrillatio
n. In this study, we investigated how dynamic factors and fixed electrophys
iological heterogeneity interact to promote wave break in simulated two-dim
ensional cardiac tissue, by using the Luo-Rudy (LR1) ventricular action pot
ential model. The degree of dynamic instability of the action potential mod
el was controlled by varying the maximal amplitude of the slow inward Ca2current to produce spiral waves in homogeneous tissue that were either near
ly stable, meandering, hypermeandering, or in breakup regimes. Fixed electr
ophysiological heterogeneity was modeled by randomly varying action potenti
al duration over different spatial scales to create dispersion of refractor
iness. We found that the degree of dispersion of refractoriness required to
induce wave break decreased markedly as dynamic instability of the cardiac
model increased. These findings suggest that reducing the dynamic instabil
ity of cardiac cells by interventions, such as decreasing the steepness of
action potential duration restitution, may still have merit as an antifibri
llatory strategy.